Abstract:
:Morphine is one of the most prescribed and effective drugs used for the treatment of acute and chronic pain conditions. In addition to its central effects, morphine can also produce peripheral analgesia. However, the mechanisms underlying this peripheral action of morphine have not yet been fully elucidated. Here, we show that the peripheral antinociceptive effect of morphine is lost in neuronal nitric-oxide synthase null mice and that morphine induces the production of nitric oxide in primary nociceptive neurons. The activation of the nitric-oxide pathway by morphine was dependent on an initial stimulation of PI3Kgamma/AKT protein kinase B (AKT) and culminated in increased activation of K(ATP) channels. In the latter, this intracellular signaling pathway might cause a hyperpolarization of nociceptive neurons, and it is fundamental for the direct blockade of inflammatory pain by morphine. This understanding offers new targets for analgesic drug development.
journal_name
Proc Natl Acad Sci U S Aauthors
Cunha TM,Roman-Campos D,Lotufo CM,Duarte HL,Souza GR,Verri WA Jr,Funez MI,Dias QM,Schivo IR,Domingues AC,Sachs D,Chiavegatto S,Teixeira MM,Hothersall JS,Cruz JS,Cunha FQ,Ferreira SHdoi
10.1073/pnas.0914733107subject
Has Abstractpub_date
2010-03-02 00:00:00pages
4442-7issue
9eissn
0027-8424issn
1091-6490pii
0914733107journal_volume
107pub_type
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